Atorvastatin Represses the Angiotensin 2-Induced Oxidative Stress and Inflammatory Response in Dendritic Cells via the PI3K/Akt/Nrf 2 Pathway
Figure 3
PI3K/Akt/Nrf 2 pathway activation mediates the protective effect of atorvastatin in BMDCs. (a) Atorvastatin promotes Akt phosphorylation in a time-dependent manner. BMDCs were treated with 10 μM atorvastatin for the indicated times. β-Actin was employed as a loading control. The graph represents the means ± (SD) (), versus time 0 min; # versus time 15 min. (b) The nuclear translocation of Nrf 2 was mediated by PI3K/Akt signals in atorvastatin-treated cells. BMDCs were treated with 100 nM Ang 2 in the presence or absence of 10 μM atorvastatin. Cellular cytoplasmic extracts (CE) and nuclear extracts (NE) were separated on a 12% SDS-PAGE gel to probe Nrf 2 and actin levels by western blotting. Total extracts of the cells were prepared, and the p-Akt (Ser473) expression was assayed by western immunoblotting. In the presence of 100 nM LY294002, the effects of atorvastatin on both Akt phosphorylation and Nrf 2 translocation were inhibited. (c) Nrf 2 activation was involved in the atorvastatin-mediated inhibition of Ang 2-induced oxidative stress. Atorvastatin induced the translocation of Nrf 2 into the nucleus and the phosphorylation of Akt. However, with 10 μM SUL, we observed only Nrf 2 activation and not Akt phosphorylation. β-Actin was employed as a loading control. The data represent the means ± SD () from three independent repeats; versus control; # versus Ang 2 + atorvastatin group.
